Alderman Michael, Aiyer Kala J V
Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, NY 10461-1602, USA.
Curr Med Res Opin. 2004 Mar;20(3):369-79. doi: 10.1185/030079904125002982.
A substantial body of epidemiological and experimental evidence suggests that serum uric acid is an important, independent risk factor for cardiovascular and renal disease especially in patients with hypertension, heart failure, or diabetes. Elevated serum uric acid is highly predictive of mortality in patients with heart failure or coronary artery disease and of cardiovascular events in patients with diabetes. Further, patients with hypertension and hyperuricemia have a 3- to 5-fold increased risk of experiencing coronary artery disease or cerebrovascular disease compared with patients with normal uric acid levels. Although the mechanisms by which uric acid may play a pathogenetic role in cardiovascular disease is unclear, hyperuricemia is associated with deleterious effects on endothelial dysfunction, oxidative metabolism, platelet adhesiveness, hemorheology, and aggregation. Xanthine oxidase inhibitors (e.g., allopurinol) or a variety of uricosuric agents (e.g., probenecid, sulfinpyrazone, benzbromarone, and benziodarone) can lower elevated uric acid levels but it is unknown whether these agents reversibly impact cardiovascular outcomes. However, the findings of the recent LIFE study in patients with hypertension and left ventricular hypertrophy suggest the possibility that a treatment-induced decrease in serum uric acid may indeed attenuate cardiovascular risk. LIFE showed that approximately 29% (14% to 107%, p = 0.004) of the treatment benefit of a losartan-based versus atenolol-based therapy on the primary composite endpoint (death, myocardial infarction, or stroke) may be ascribed to differences in achieved serum uric acid levels. Overall, serum uric acid may be a powerful tool to help stratify risk for cardiovascular disease. At the very least, it should be carefully considered when evaluating overall cardiovascular risk.
大量的流行病学和实验证据表明，血清尿酸是心血管和肾脏疾病的一个重要的独立危险因素，尤其在高血压、心力衰竭或糖尿病患者中。血清尿酸升高高度预示着心力衰竭或冠状动脉疾病患者的死亡率以及糖尿病患者的心血管事件。此外，与尿酸水平正常的患者相比，高血压和高尿酸血症患者发生冠状动脉疾病或脑血管疾病的风险增加3至5倍。尽管尿酸在心血管疾病中发挥致病作用的机制尚不清楚，但高尿酸血症与对内皮功能障碍、氧化代谢、血小板黏附性、血液流变学和聚集的有害影响有关。黄嘌呤氧化酶抑制剂（如别嘌醇）或多种促尿酸排泄剂（如丙磺舒、磺吡酮、苯溴马隆和苄碘达隆）可降低升高的尿酸水平，但这些药物是否能可逆地影响心血管结局尚不清楚。然而，最近针对高血压和左心室肥厚患者的LIFE研究结果表明，治疗引起的血清尿酸降低可能确实会减轻心血管风险。LIFE研究表明，基于氯沙坦与基于阿替洛尔的治疗在主要复合终点（死亡、心肌梗死或中风）上的治疗益处中，约29%（14%至107%，p = 0.004）可能归因于所达到的血清尿酸水平的差异。总体而言，血清尿酸可能是帮助分层心血管疾病风险的有力工具。至少，在评估整体心血管风险时应仔细考虑血清尿酸。
